Aging is characterized by reductions in the amplitude of a wide variety of circadian rhythms in mammals. This is particularly evident in the daily patterns of sleep and wakefulness which becomes progressively fragmented in the later years of life. The ubiquity of age-related decrements in circadian timekeeping and evidence of morphological changes in the suprachiasmatic nuclei (SCN) with age have contributed to the current view that age-related sleep-wake cycle fragmentation is due to organic deterioration of the biological clock. There are, however, at least two processes involved in sleep-wake cycle regulation -- a circadian process that appears to promote wakefulness at specific times of the day, and a sleep homeostatic process responsible for compensatory sleep in response to clock-imposed prior wakefulness. Age-related deterioration in sleep-wake cycle regulation may therefore involve intrinsic oscillatory mechanisms of the SCN, SCN effector mechanisms responsible for promoting wakefulness, and/or the sleep homeostat. Our recent investigations lead us to believe that age-related fragmentation of the sleep/wake cycle may be due to both deterioration in the circadian and homeostatic process controlling sleep-wakefulness. Little is known about how the circadian clock modulates states of arousal. Within the framework of an Opponent Process Model of sleep/wake regulation, we plan to investigate both the circadian and homeostatic control of sleep as a function of aging primarily using longitudinal experimental designs. Experiments will involve much needed longitudinal sleep-wake recordings under constant environmental conditions to accurately characterize circadian rhythm decrements with aging. SCN- lesioned rats will be subjected to acute sleep deprivation to assay age- related decrements of the sleep homeostatic process independent of influences from the circadian clock. We will also employ fetal SCN- transplantation techniques to restore sleep-wake cycles in SCN-lesioned and aged rats to further characterize the functional role of the SCN in sleep-wake regulation, and to determine if attributes of the transplanted SCN can ameliorate age-related sleep-wake regulation, and to determine if attributes of the transplanted SCN can ameliorate age-related sleep- wake cycle fragmentation. Finally, we will microinject anesthetics, tetrodotoxin, and GABA agonists/antagonists into the SCN or transplanted SCN to better understand how the circadian clock communicates temporal information that enhances sleep-wake cycle consolidation. These experiments should greatly improve our understanding of circadian and homeostatic determinants of sleep-wakefulness and their roles in age- related fragmentation of the sleep-wake cycle.